Abstract
Background TWEAK, MCP-1 and NGAL, mediators in pathogenesis of systemic lupus erythematosus (SLE), are proinflammatory cytokines/chemokines that are thought as potential biomarkers reflecting disease activity. In this study, we aimed to investigate the association of serum (s) and urine (u) levels of TWEAK, MCP-1 and NGAL with disease activity in both renal and non-renal SLE.
Methods Thirty active patients with SLE (15 renal and 15 non-renal) were recruited. Thirty-one inactive patients with SLE (16 renal and 15 non-renal), 14 patients with ANCA-associated vasculitis (AAV) all of whom had active renal involvement and 20 healthy volunteers were selected as control groups. Serum and urine levels of TWEAK, MCP-1 and NGAL were tested using ELISA.
Results Sixty-one SLE patients, 51 (83.6%) of whom were female, with a median disease duration of 83 (23.5–135) months and a median age of 35 (27–47.5) were included in the study. Serum and urine levels of TWEAK and NGAL were significantly higher in the active SLE group compared with the inactive SLE (n=31) group (sTWEAK: p=0.005; uTWEAK: p=0.026; sNGAL: p<0.001; uNGAL: p=0.002); whilst no significant differences regarding serum and urine MCP-1 levels were observed (p=0.189 and p=0.106). uTWEAK (p=0.237), sMCP-1 (p=0.141), uMCP-1 (p=0.206), sNGAL (p=0.419) and uNGAL (p=0.443) levels did not differ between patients with active LN and non-renal active SLE; yet levels of sTWEAK were higher in patients with active LN (p=0.006). There were no differences between active LN and renal active AAV. Levels of all biomarkers were correlated with SLEDAI (sTWEAK: p=0.001; uTWEAK: p=0.006; sMCP-1: p=0.049; uMCP-1: p=0.014; sNGAL: p<0.001; uNGAL: p=0.002).
Conclusions sTWEAK, uTWEAK, sNGAL and uNGAL are significant biomarkers showing disease activity in SLE. However, our results implicate that these biomarkers may not be specific for SLE, and can be elevated in patients with active renal involvement of AAV. sTWEAK may be of use for discriminating active nephritis from non-renal active disease in SLE. Further studies are awaited to confirm these Results
Funding Source(s): This study was funded by Istanbul University with the project number TTU-2017–24 738